1. Field of the Invention
The present invention relates to a food composition for removing amyloid plaques, the food composition including ginsenoside F1 or a sitologically acceptable salt thereof. Further, the present invention relates to a feed composition for removing amyloid plaques, the feed composition including ginsenoside F1 or a sitologically acceptable salt thereof. Furthermore, the present invention relates to a method of removing amyloid plaques, the method including the step of administering ginsenoside F1 to a subject excluding humans.
2. Description of the Related Art
Alzheimer's dementia is a disease that most frequently occurs in the elderly, and about 10% of the population of 65-85 years of age and about 40% of the population over 85 years of age suffer this disease. Alzheimer's dementia was reported at first by the observation of Alois Alzheimer of Germany in 1907, and he observed that nerve cells of hippocampus and neocortex of the brain of Alzheimer's patients were lost and there were abnormal structures such as neurofibrillary tangles (NTFs) which look like tangled bundles of fiber and senile plaques within the cell body of neurons.
Of them, senile plaques, also called amyloid plaques, are extracellular deposits of amyloid peptide surrounded by neuritis, astrocytes, microglial cells or the like, and are found mainly in the limbic structure or association neocortex.
Many studies have been conducted to investigate whether these abnormal tissue properties relate to the pathogenesis of dementia.
Specifically, sporadic Alzheimer's disease (SAD) accounts for most cases of dementia, but there have been no findings supporting that SAD is caused by particular genetic mutations. However, senile plaques and neurofibrillary tangles regarded as the pathological features of dementia are found in patients with sporadic dementia. In particular, excess deposition of beta amyloid protein is commonly found in sporadic dementia and hereditary dementia, suggesting that beta amyloid is presumed to play a major role in the pathogenesis of dementia (Nature, 1999, 399:A23-A31).
Now, on the basis of this, global pharmaceutical companies have been focused on therapeutic agents targeting beta amyloid plaques. However, the therapeutic agents developed until now have weak, temporary efficacy and they also show severe toxicity. There have been few case reports regarding successful clinical trials.
Accordingly, the present inventors have made many efforts to develop a substance capable of removing amyloid plaques which is a cause of Alzheimer's dementia. As a result, they found that a natural substance, ginsenoside F1 has a very excellent effect of removing amyloid plaques, thereby completing the present invention.